The early work of Hamilton and colleagues (Am J Physiol 1944; 141:235-41) during World War 2 showed the differences in pressure waveforms that are seen in hypotension, and how hypotension associated with vasodilation and secondary shock was associated with damped pressure waveforms and small or absent diastolic pressure fluctuations—see FIG. 1.
Subsequent work (O'Rourke M F, Am Heart J 1971; 82:687-702, Nichols and O'Rourke, McDonald's Blood Flow in Arteries; Arnold, London 1998 p. 170-189) (FIG. 2) has shown repeatedly in humans and experimental animals, that acute blood loss or fall in cardiac output from other causes is associated with amplification of the peripheral pressure wave, with prominence in the diastolic components of these waves—See FIG. 2. This was attributed to a combination of vasoconstriction, causing increased wave reflection, together with shortening of systole caused by tachycardia, such that secondary pressure waves became unusually prominent.
Further studies on frequency components of the pressure and flow waveforms confirmed these explanations and raised the possibility that automatic methods could be applied to pressure waves to distinguish uncomplicated from complicated shock through identification of change in frequency components of the pressure waves as well as from change in the secondary fluctuations of the waveforms in the time domain.